Cell Signaling Technology

Caveolin-1 (D46G3) Rabbit Monoclonal Antibody

#3267 · $161

100
Citing papers
11.7k
Combined citations
Supplier page Find this product

Research areas

MicroRNA in disease regulation9Cancer, Hypoxia, and Metabolism8Chemotherapy-induced cardiotoxicity and mitigation5Cancer Cells and Metastasis5HER2/EGFR in Cancer Research5PI3K/AKT/mTOR signaling in cancer5Epigenetics and DNA Methylation4Extracellular vesicles in disease4

Papers citing this product

1
Oncogenic Transformation by Inhibitor-Sensitive and -Resistant EGFR Mutants
PLoS Medicine·2005·683 cit.·DOI
2
AXL is a candidate receptor for SARS-CoV-2 that promotes infection of pulmonary and bronchial epithelial cells
Cell Research·2021·507 cit.·DOI
3
FNDC5 alleviates oxidative stress and cardiomyocyte apoptosis in doxorubicin-induced cardiotoxicity via activating AKT
Cell Death and Differentiation·2019·447 cit.·DOI
4
Epithelial–Mesenchymal Transition (EMT) Induced by TNF-α Requires AKT/GSK-3β-Mediated Stabilization of Snail in Colorectal Cancer
PLoS ONE·2013·276 cit.·DOI
5
The Ca2+-dependent protein kinase CPK3 is required for MAPK-independent salt-stress acclimation in Arabidopsis
The Plant Journal·2010·275 cit.·DOI
6
The Nlrp3 inflammasome regulates acute graft-versus-host disease
The Journal of Experimental Medicine·2013·233 cit.·DOI
7
A phase I dose escalation study of BIBW 2992, an irreversible dual inhibitor of epidermal growth factor receptor 1 (EGFR) and 2 (HER2) tyrosine kinase in a 2-week on, 2-week off schedule in patients with advanced solid tumours
British Journal of Cancer·2007·231 cit.·DOI
8
miR-23b-3p regulates the chemoresistance of gastric cancer cells by targeting ATG12 and HMGB2
Cell Death and Disease·2015·219 cit.·DOI
9
Mutual dependence of the MRTF–SRF and YAP–TEAD pathways in cancer-associated fibroblasts is indirect and mediated by cytoskeletal dynamics
Genes & Development·2017·206 cit.·DOI
10
Activation of NLRP3 inflammasome enhances the proliferation and migration of A549 lung cancer cells
Oncology Reports·2016·194 cit.·DOI

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